| Summary: | Mastitis is a syndrome manifested by mammary gland inflammation which is thought to cause between $300 and $400 million in annual losses to the Canadian Dairy Industry. Studies have indicated that <i>S. aureus</i> may cause the production of anti-inflammatory cytokines which may enhance its survival within the bovine mammary gland. However, other studies have reported differing results following S. aureus intramammary infection (IMI). This thesis tested the hypothesis that S. aureus generated anti-inflammatory cytokine responses at the site of infection. In the first objective, different S. aureus isolates were screened for their effects on cytokine production (IFN-γ, TNF-α, IL-4 and IL-10) by bovine peripheral blood mononuclear cells (PBMCs) in vitro. Nine S. aureus isolates were co-cultured with PBMCs from lactating dairy cattle. Cattle used in the study had recall immune responses to <i>S. aureus</i>. The majority (6/9) of S. aureus isolates had minor effectors on cytokine production. The three remaining isolates generated large cytokine responses with both pro-inflammatory (IFN-γ and TNF-α) and anti-inflammatory (IL-4 and IL-10) characteristics. Two of these three isolates were tested in vivo by experimentally infecting lactating ewes. Cytokine production was characterized in the teat end, the mammary parenchyma and the supramammary lymph nodes (SMLNs). One isolate generated anti-inflammatory responses <i>in vivo</i> (IL-4 and IL-10) whilst the other generated both pro-inflammatory (IFN-γ) and anti-inflammatory (IL-10) responses in vivo. Given that some studies have suggested a role of staphylococcal enterotoxin C (sec) in the generation of anti-inflammatory responses, the role of sec was also investigated using bovine PBMCs. When purified SEC protein was co-cultured with PBMCs from beef steers, anti-inflammatory cytokines were produced. However, a <i>S. aureus</i> strain which was transformed for the sec gene did not affect cytokine production when co-cultured with PBMCs from lactating dairy cattle. The results of this thesis suggest that <i>S. aureus</i> infection can cause anti-inflammatory cytokine production but the response depends on the isolate causing the infection. Furthermore, the role of sec appears to be minimal.
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